Cellular and Developmental Biology MRes/PhD Supervisors
- Steve Alexander (Endogenous cannabinoid system, with particular focus on inflammation and pain).
- Steve Briddon (Molecular Pharmacology of G protein-coupled receptors and advanced fluorescence imaging)
- William Brown (Chromosome biology)
- Meritxell Canals (G protein-coupled receptor signalling and drug-screening with a focus on inflammation and pain).
- Federico Dajas-Bailador (Neurons, RNA, Translation, miRNAs, neurodegeneration, pain)
- Claire Friel (biochemistry, biophysics, proteins, cytoskeleton, cell division, neurodegeneration, microscopy, optical trapping). Research in the Friel lab utilises fundamental biomolecular insights to uncover the molecular mechanisms underlying cellular systems and disease. We have a focus on the dynamics and regulation of cytoskeletal filaments. Using advanced biochemical and biophysical approaches, we seek to elucidate the core molecular principles governing filament function and connect these findings to complex cellular processes such as cell division and nervous system function.
- Marios Georgiou (Cancer biology; Cell morphogenisis).
- Alan Huett (The role of autophagy in sensing and controlling bacterial infection).
- Alistair Hume (Organelles and disease).
- Ian Kerr (ATP binding cassette transporters, membrane protein expression and purification, transmembrane transport, enzymes in pain processing, paediatric brain tumour cell biology, extracellular vesicles).
- Yan Liao My research focuses on understanding the molecular mechanisms that archaeal cells use for adaptation, interaction, and division, and on developing these systems for novel biotechnological applications relevant to environmental and human health.
- Rob Lane (Neuropharmacology of G protein-coupled receptor (GPCRs) function and signalling).
- Naomi Martin (cancer immunology, immune evasion, flow cytometry, immune dysfunction, endothelial dysfunction, extracellular vesicles). Recently, I have been working on projects investigating mechanisms of cancer immune evasion and the effects of stressed and metastatic cancer cells on the phenotype of neighbouring healthy cells in in vitro co-cultures.My research also investigates the function of extracellular vesicles in disease processes such as cancer and cardiovascular disease and their role in the susceptibility of certain ethnic groups to these diseases. I investigate how these novel markers of immune function and inflammation are altered phenotypically and their effects on disease pathophysiology and cellular dysfunction. I also have an interest in the effects of polluting microplastics on cancer progression and pathophysiology and cellular dysfunction.
- Chloe Peach (receptor tyrosine kinase (RTK) signalling, studying how they are modulated by growth factors, drugs or their local microenvironment, with a focus on neuronal regeneration). Despite major advances in our understanding of human biology, over 90% of drugs fail in patients. Many drugs target receptors, as membrane proteins that detect extracellular stimuli and evoke intracellular responses. RTKs are a family of 58 membrane proteins that respond to growth factors. These large ligands trigger signalling cascades that lead to cell proliferation, avoidance of cell death and initiation of migratory processes. They are therefore major targets in the field of oncology, however RTKs have wide-reaching pathological implications. Neurotrophins, for example, are a family of growth factors that stimulate neuronal growth. These growth factors, as well as their receptors, are promising targets for the treatment of neurodegenerative disease (agonists) or chronic pain (antagonists), however they lack clinically approved drugs.
- Andrew Renault (Drosophila, germ cells, cell migration, embryogenesis)
- Rita Tewari (Functional analysis of signalling pathways modulating malaria parasite development, cell division and parasite proliferation).
- Rebecca Trueman (Myotonic Dystrophy; RNA repeat expansion disorders; Drug discovery). My research group investigates the pathological mechanisms of myotonic dystrophy, with a particular focus on developing novel therapeutic approaches and on understanding how this disease impacts the brain. Combining neuroscience, cell biology and translational medicine, we aim it have in impact on patients lives.
- Uwe Vinkemeier (Neuroimmunology and cytokine-regulation of STAT transcriptional activity in the immune system).
- Sally Wheatley (mitosis, cytokinesis, mitochondria, survivin, cancer, cytoskeleton, biochemistry, cell biology, microscopy) My work focusses on a small protein called "survivin" that is involved in many cellular processes. It has been extensively studied by oncologists as it is highly overexpressed in all cancers. However, it is not an enzyme, and so targetting it for therapeutic gain has not been hugely successful. Survivin does everything in collaboration - its interactome is vast and list of interactors ever increasing. Found in different parts of the cell at different times, as a chromosomal passenger protein, survivin is essential for mitosis and cytokinesis, but it is also an inhibitor of apoptosis (IAP) and its presence in the cytoplasm correlates with poor repsonse to chemo and radiation therapies. More recently, it has become appreciated that when it is in the nucleus it can alter transcriptional programming, and this seems to have relevance to cells experience stress such as hypoxia. In identifying novel survivin interactors, we hope to find an association that could be targetted for therapeutic purposes.
Developmental Biology Supervisors
- Federico Dajas-Bailador (Neurons, RNA, Translation, miRNAs, neurodegeneration, pain).
- Angus Davison (Evolution, Genetics, Snails, Genomics, Bioinformatics, Colour, Asymmetry).
- Martin Gering (Embryonic haematopoiesis in zebrafish).
- Tom Hartman (Protists, Microscopy, palaeontology, chromosomes, genome size, meiosis, natural history, photography, 3D scanning).
- Matt Loose (Nanopore sequencing).
- Siobhan Loughna (CHD, congenital heart disease, heart defects, Prkd1, Cdk13, pathogenic variants, humanised transgenic mutant mouse, high resolution episcopic microscopy). Our research interests are to provide insights into how the heart forms during early stages of cardiogenesis, and how it goes wrong leading to defects. Congenital heart disease is relatively common (approximately 0.8% of newborn babies), with most cases having an unknown cause. In collaboration with Professor David Brook, we have analysed a number of mouse lines which carry deletions or humanised mutations for genes which are know to cause heart defects in humans. Our current genes of interest are Cdk13 and Prkd1, with both encoding a protein kinase. Mutations in these genes result in congenital heart disease. Morphological analysis is by high resolution episcopic microscopy (HREM), which allows 2D and 3D analysis of the hearts. A range of developmental, cell and molecular biology techniques are employed in the laboratory to decipher the expression of these genes of interest and understand the abnormalities seen. Further, functional studies are performed to provide insights into what role the genes play in the heart in order to explain how defects form.
- Chloe Peach (receptor tyrosine kinase (RTK) signalling, studying how they are modulated by growth factors, drugs or their local microenvironment, with a focus on neuronal regeneration). Despite major advances in our understanding of human biology, over 90% of drugs fail in patients. Many drugs target receptors, as membrane proteins that detect extracellular stimuli and evoke intracellular responses. RTKs are a family of 58 membrane proteins that respond to growth factors. These large ligands trigger signalling cascades that lead to cell proliferation, avoidance of cell death and initiation of migratory processes. They are therefore major targets in the field of oncology, however RTKs have wide-reaching pathological implications. Neurotrophins, for example, are a family of growth factors that stimulate neuronal growth. These growth factors, as well as their receptors, are promising targets for the treatment of neurodegenerative disease (agonists) or chronic pain (antagonists), however they lack clinically approved drugs.
- Andrew Renault (Drosophila, germ cells, cell migration, embryogenesis).
- Rita Tewari (Functional analysis of signalling pathways modulating malaria parasite development, cell division and parasite proliferation).
Stem Cell Biology Supervisors
- Martin Gering (Embryonic haematopoiesis in zebrafish).
- Andrew Renault (Drosophila, germ cells, cell migration, embryogenesis).
- Daniel Scott Utilising iPSC models we study the cellular and molecular mechanisms of Motor neurone diseases.
- Sebastian Serres (metabolism, brain, imaging, astrocyte, tracer).
Molecular Cell Biology Supervisors
- Steve Alexander (Endogenous cannabinoid system, with particular focus on inflammation and pain).
- Andrew Bennett (Neuroinflammation and metabolic dysfunction).
- William Brown (The genetics and evolution of centromere assembly in vertebrates and fission yeast; Human mini-chromosome engineering).
- Federico Dajas-Bailador (Neurons, RNA, Translation, miRNAs, neurodegeneration, pain).
- Claire Friel (biochemistry, biophysics, proteins, cytoskeleton, cell division, neurodegeneration, microscopy, optical trapping). Research in the Friel lab utilises fundamental biomolecular insights to uncover the molecular mechanisms underlying cellular systems and disease. We have a focus on the dynamics and regulation of cytoskeletal filaments. Using advanced biochemical and biophysical approaches, we seek to elucidate the core molecular principles governing filament function and connect these findings to complex cellular processes such as cell division and nervous system function.
- Marios Georgiou (Cancer biology; Cell morphogenisis).
- Alistair Hume (Organelles and disease).
- Ian Kerr (ATP binding cassette transporters, membrane protein expression and purification, transmembrane transport, enzymes in pain processing, paediatric brain tumour cell biology, extracellular vesicles).
- Robert Layfield (MND mechanisms; ancient proteins; proteomics; protein science).
- Yan Liao My research focuses on understanding the molecular mechanisms that archaeal cells use for adaptation, interaction, and division, and on developing these systems for novel biotechnological applications relevant to environmental and human health.
- Lopa Leach (Regulation of vascular flow and barrier function in the human placenta in normal and compromised pregnancies).
- Andrew Renault (Drosophila, germ cells, cell migration, embryogenesis).
- Rita Tewari (Functional analysis of signalling pathways modulating malaria parasite development, cell division and parasite proliferation).
- Daniel Scott Utilising iPSC models we study the cellular and molecular mechanisms of Motor neurone diseases.
- Uwe Vinkemeier (Cytokines; Signal transduction in myeloid cells).
- Sally Wheatley (mitosis, cytokinesis, mitochondria, survivin, cancer, cytoskeleton, biochemistry, cell biology, microscopy) My work focusses on a small protein called "survivin" that is involved in many cellular processes. It has been extensively studied by oncologists as it is highly overexpressed in all cancers. However, it is not an enzyme, and so targetting it for therapeutic gain has not been hugely successful. Survivin does everything in collaboration - its interactome is vast and list of interactors ever increasing. Found in different parts of the cell at different times, as a chromosomal passenger protein, survivin is essential for mitosis and cytokinesis, but it is also an inhibitor of apoptosis (IAP) and its presence in the cytoplasm correlates with poor repsonse to chemo and radiation therapies. More recently, it has become appreciated that when it is in the nucleus it can alter transcriptional programming, and this seems to have relevance to cells experience stress such as hypoxia. In identifying novel survivin interactors, we hope to find an association that could be targetted for therapeutic purposes.